Thyroid vascularization by color doppler ultrasonography in Graves' disease. Changes related to different phases and to the long-term outcome of the disease.
To investigate possible correlations between thyroid vascularization and activity of Graves' disease, we measured blood flow (TBF) at the inferior thyroid artery and intraparenchymal vascularization (number of vessels per square centimeter) by color Doppler ultrasonography (CDU) on Graves' patients at different phases of the disease. We studied 88 patients cross sectionally: 22 untreated; 17 euthyroid after 6 months of methimazole; 49 euthyroid at drug withdrawal after 12 to 24 months of treatment. The patients of the latter group were followed up for 29.1 +/- 6.3 months after discontinuation of treatment. On the day of CDU examination, free triiodothyronine (FT3), free thyroxine (FT4), thyrotropin (TSH), antiperoxidase and anti-TSH receptor (TRAb) antibodies were measured. Vascularization indices were significantly higher in the Graves' patients than in controls. In the patients euthyroid under treatment, vascularization was not significantly lower than in the untreated group, but TBF and vessel number both appeared clearly reduced in the patients tested at drug withdrawal. The vascularization indices at drug withdrawal were significantly higher in the patients who relapsed than in those in stable remission: TBF (mL/min) 50.6 +/- 36.8 vs. 23.8 +/- 17.5, p = 0.001; vessel number/cm2 1.8 +/- 0.8 vs. 0.8 +/- 0.5, p = 0.002. A multivariate analysis, evaluating the predictive value of vascularization, hormonal and immunological parameters for relapse, demonstrated a significant predictive value for TRAb (RR 8.2; p = 0.001) and a weak predictive value for TBF (RR 1.1; p = 0.02). In conclusion, CDU examination confirms that thyroid hypervascularization in Graves' disease is not related to thyroid hormone circulating levels. The association of increased TBF and high levels of TRAb in the relapsing forms of disease suggests that thyroid hypervascularization is probably related to the activity of the underlying autoimmune processes.
Baldini
M
M
Istituto di Medicina Interna, Malattie Infettive e Immunopatologia dell'Università di Milano, IRCCS Ospedale Maggiore di Milano, Italy.
Castagnone
D
D
Rivolta
R
R
Meroni
L
L
Pappalettera
M
M
Cantalamessa
L
L
D000328:Adult; D000368:Aged; D000906:Antibodies / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D013956:Antithyroid Agents / Q000627:therapeutic use; D001158:Arteries / Q000000981:diagnostic imaging; D005260:Female; D006111:Graves Disease / Q000000981:diagnostic imaging* / Q000188:drug therapy / Q000473:pathology; D006728:Hormones / Q000097:blood; D006801:Humans; D007453:Iodide Peroxidase / Q000276:immunology; D008297:Male; D008713:Methimazole / Q000627:therapeutic use; D008875:Middle Aged; D009929:Organ Size; D011379:Prognosis; D011989:Receptors, Thyrotropin / Q000276:immunology; D012008:Recurrence; D012039:Regional Blood Flow; D013961:Thyroid Gland / Q000098:blood supply* / Q000000981:diagnostic imaging* / Q000187:drug effects; D013972:Thyrotropin / Q000187:drug effects / Q000378:metabolism; D013974:Thyroxine / Q000187:drug effects / Q000378:metabolism; D013997:Time Factors; D016896:Treatment Outcome; D014284:Triiodothyronine / Q000187:drug effects / Q000378:metabolism; D018615:Ultrasonography, Doppler, Color
D000906:Antibodies; D013956:Antithyroid Agents; D006728:Hormones; D011989:Receptors, Thyrotropin; D014284:Triiodothyronine; D008713:Methimazole; D013972:Thyrotropin; D007453:Iodide Peroxidase; D013974:Thyroxine